Anders Palmstrøm Jørgensen1, Thor Ueland2, Rasmus Sode-Carlsen3, Thomas Schreiner4, Kai Fredrik Rabben5, Stense Farholt3, Charlotte Høybye6, Jens Sandahl Christiansen7, Jens Bollerslev8. 1. Section of Specialized Endocrinology, Department of Endocrinology, Oslo University Hospital, Rikshospitalet, Oslo, Norway. Electronic address: andjoe@ous-hf.no. 2. Research Institute for Internal Medicine, Faculty of Medicine, University of Oslo, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway. 3. Centre for Rare Diseases, Department of Pediatrics, Aarhus University Hospital Skejby, Aarhus N, Denmark. 4. Section of Specialized Endocrinology, Department of Endocrinology, Oslo University Hospital, Rikshospitalet, Oslo, Norway. 5. Frambu, Siggerud, Norway. 6. Department of Endocrinology, Metabolism and Diabetology, Karolinska University Hospital, Stockholm, Sweden. 7. Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus C, Denmark. 8. Section of Specialized Endocrinology, Department of Endocrinology, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway.
Abstract
OBJECTIVES: To investigate glucose homeostasis in relation to body mass index (BMI) in adults with PWS before and after GH therapy. DESIGN: We prospectively investigated the effects of a 12-month GH treatment on body composition and glucose homeostasis in relation to BMI in 39 adults, mean (±SD) age=28.6 (6.5) years with genetically verified PWS. We compared the results for different BMI categories (<25 kg/m²; 25-30 kg/m²; >30 kg/m²) and performed a regression analysis to detect predictors for homeostasis model of assessment-insulin resistance (HOMA-IR). RESULTS: The baseline HOMA-IR was higher, with BMI of >30 kg/m². Our main findings were as follows: i) GH treatment (mean final dose, 0.6 (0.25) mg) was associated with small increases in fasting p-glucose, 2-h p-glucose by oral glucose load tolerance test, HOMA-IR and lean mass, and a reduction in fat mass. ii) Whereas the baseline HOMA-IR was associated with increased BMI (>30 kg/m²), we found no differences in HOMA-IR among the BMI categories after 12 months of GH. iii) Stepwise linear regression identified the triglyceride level as the strongest predictor of HOMA-IR at baseline, whereas an increase in VAT was the strongest predictor of the increase in HOMA-IR after therapy. CONCLUSIONS: GH treatment for 12 months in adults with PWS resulted in an increase in HOMA-IR, irrespective of BMI, confirming that control of HbA1c is essential during GH treatment in PWS.
OBJECTIVES: To investigate glucose homeostasis in relation to body mass index (BMI) in adults with PWS before and after GH therapy. DESIGN: We prospectively investigated the effects of a 12-month GH treatment on body composition and glucose homeostasis in relation to BMI in 39 adults, mean (±SD) age=28.6 (6.5) years with genetically verified PWS. We compared the results for different BMI categories (<25 kg/m²; 25-30 kg/m²; >30 kg/m²) and performed a regression analysis to detect predictors for homeostasis model of assessment-insulin resistance (HOMA-IR). RESULTS: The baseline HOMA-IR was higher, with BMI of >30 kg/m². Our main findings were as follows: i) GH treatment (mean final dose, 0.6 (0.25) mg) was associated with small increases in fasting p-glucose, 2-h p-glucose by oral glucose load tolerance test, HOMA-IR and lean mass, and a reduction in fat mass. ii) Whereas the baseline HOMA-IR was associated with increased BMI (>30 kg/m²), we found no differences in HOMA-IR among the BMI categories after 12 months of GH. iii) Stepwise linear regression identified the triglyceride level as the strongest predictor of HOMA-IR at baseline, whereas an increase in VAT was the strongest predictor of the increase in HOMA-IR after therapy. CONCLUSIONS: GH treatment for 12 months in adults with PWS resulted in an increase in HOMA-IR, irrespective of BMI, confirming that control of HbA1c is essential during GH treatment in PWS.